In order to better understand cardiac dysfunctions such as cardiomyopathies and valvulopathies, object of the treatment and which affect the heart, we will provide a brief description of the heart structure and function.
The heart comprises cavities which communicate with one another and with the venous and arterial system through valves. In the case in question, the heart comprises four cavities: a right atrium, a left atrium, a right ventricle, and a left ventricle; and four valves: the mitral valve, the aortic valve, the pulmonary valve and the tricuspid valve. The blood from the human body transits through the right atrium and from here crosses through the tricuspid valve, to the right ventricle which pumps the blood to the lungs through the pulmonary artery. The right ventricle is separated from the pulmonary artery by the pulmonary valve which regulates the flow. The oxygenated blood from the lungs is fed through the pulmonary veins, to the left atrium, which communicates with the left ventricle through the mitral valve. The left ventricle feeds the oxygenated blood to the human body through the aorta, from which it is separated by the aortic valve.
The pumping action of the blood is performed by the right ventricle and the left ventricle, the walls of which are defined, at least partially, by the cardiac muscle that determines in succession, the diastolic phases, in other words the dilatation phases of the right and left ventricles with relative blood filling, with intervals of systolic phases, or contraction phases of the right and left ventricles with relative expulsion of the blood from the ventricles in question.
The term heart failure defines a physiopathological state wherein the heart is not able to pump the blood in sufficient quantities for the metabolic requirements of the tissues, or wherein it performs a pumping action with excessively high filling pressure.
Heart failure can generally be determined by a dilative cardiomiopathy, in other words, a dysfunction of the cardiac muscle that reduces the efficiency of the heart in systolic phase or by a valvulopathy, in other words, affection of at least one of the cardiac valves: the mitral valve, the aortic valve, the tricuspid valve, or the pulmonary valve. In mechanical terms, the valves play a fundamental role in regulating the flow and must work in perfect synchronization with diastolic and systolic succession.
The opening and closing action of the cardiac valves is mainly determined by the pressure level upstream and downstream of the valve and by the variation induced by the ventricular walls.
The mechanical function of each component of the cardiac pump (ventricular walls, structures that comprise the valves) has a physiologically elastic behaviour, and mechanical dysfunction is caused by the loss of elasticity of these components.
Alteration to elastic properties provokes dysfunctions that are generally defined as heart failures.
The most common form of heart failure of a mechanical nature is due to the excessive dilatation (dilative cardiomiopathy) of a ventricular chamber (in particular the left chamber) that can provoke a series of geometrical changes that also alter the geometry and function of the atrioventricular valve (above all the mitral valve) making it insufficient/not competent (valvulopathy).
Problems concerning heart failure are the object of many scientific publications and many patents. As far heart failure repair at valvular level is concerned, a known method is the use of constrictor rings, among which, the most well-known is the Carpentier ring. The repair technique which uses constrictor rings has been well consolidated and particular evolution in relation to constrictor rings has been the object of many patents and patent applications, among which we recall the following: U.S. Pat. No. 5,674,280 (Davidson); U.S. Pat. No. 4,164,064 (Cooley); U.S. Pat. No. 5,776189 (Kahlid); U.S. Pat. No. 6,360,749 (Jayaraman); US 2007/0016289 (Johnson); US 2004/0138745 (Macoviak); US 2006/0074484 (Huber); WO 2006/078694 (Speziali); U.S. Pat. No. 5,961,539(Northrup); US 2006/0184241 (Marquez); WO 2006/086434 (Evalve Inc.); US 2005/0065601 (Lee); and US 2003/0045929 (McCarthy).
Other patent documents, including US 2006/081968 (Duran) suggest the insertion of mechanical devices by percutaneous intervention into the interventricular veins for the treatment of heart failure at mitral level.
Other patent documents propose solutions for heart failure caused by dilatation and dysfunction by providing constricting instruments conceived to prevent any further dilatation phenomena. These patents include U.S. Pat. No. 6,264,602 (Mortier); US 2006/0004247 (Kute).
Solutions to heart failure problems have been proposed for the treatment of both cardiomyopathies and valvulopathies which use the cardiac cycle and create an exchange of energy between the cardiac structures and the intracardiac device.
Among these solutions there is that proposed by the Applicant in the patent application WO 01/078625, wherein an intracardiac device is described, comprising an elongated member, which is elastically extendable. Basically, when the intracardiac device is implanted along the equatorial plane of the ventricular or along the valvular mitral annulus, it stores elastic energy during the diastolic phase and cedes this energy during the systolic phase to the respective cardiac structure, in this particular case, the tissues that form the walls of the ventricular or valvular annulus.
This solution is also the object of publications in the JCM Journal of Cardiovascular Medicine 2006 Vol. 1 No. 00—THE TITAN CAN HELP TITIN: FROM MICRO TO MACRO MYOCARDIAL ELASTICITY.
A further article on the same subject is published in the JACC Journal of America College of Cardiology Oct. 30, 2007 Vol. 50 No. 18 2007—IMPLANTATION OF AN ELASTIC RING AT EQUATOR OF THE LEFT VENTRICLE INFLUENCES CARDIAC MECHANICS IN EXPERIMENTAL ACUTE VENTRICULAR DYSFUNCTION.
These scientific publications endorsed the validity of the basic idea and led the Applicant to researching more deeply into the structural nature of intracardiac device and its compatibility with the human organism.
Generally, the presence of an artificial body inside a cardiac cavity always provokes a reaction by the organism, consisting of the generation of a fine layer of fibrous tissue.
Live experiments performed on sheep have shown a fibrotic reaction that in certain cases provoked attachment connection hardening, and consequential unwelcome stress on the sutures. Furthermore, an excessive fibrotic reaction could reduce elasticity and compromise correct operating function.